Uterine receptivity for blastocyst implantation is time and hormone dependent. It occurs only for a limited period during pregnancy, pseudopregnancy, or when the uterus is primed by an appropriate amount of progesterone (P4) and estrogen. In the rat, uterine sensitivity can be divided into (i) neutral, (ii) receptive and (iii) nonreceptive phases. In the pregnant and pseudopregnant rat, the uterus becomes receptive only on day 5 (the day of implantation), while by day 6 it becomes refractory and fails to respond to blastocysts or other traumatic stimuli for induction of implantation or decidual response. The neutral state is achieved when the uterus is exposed to P4 only. Under this condition, although the uterus can undergo decidualization following traumatization, it does not respond to the presence of blastocysts. Such a uterus does support the blastocysts for delayed implantation. However, the uterus can be rendered receptive for blastocyst implantation, if it is exposed to a minute amount of estrogen after at least 48 h of P4 priming. The uterus then becomes refractory after 24 h. All these states of uterine sensitivity can be induced experimentally and could be used as suitable models for understanding the mechanism of implantation. A local proinflammatory type of reaction accompanied by an increased uterine stromal capillary permeability at the site of blastocyst attachment is considered to be one of the earliest discernible prerequisite events for implantation and is preceded by a generalized stromal edema. These significant events are observed only during the receptive phase. The release of histamine and prostaglandins (PGs), as an estrogen action, has been suggested to play a role in these events. The recent discovery of a new class of lipid molecules, leukotrienes (LTs), which are synthesized via 5-lipoxygenase, from the same arachidonic acid molecules from which PGs are formed, has created an intense new research interest in the field. Leukotrienes are potent vasoactive agents and mediators of various kinds of inflammatory reactions. Therefore, our objective is to study the role of PGs and LTs in implantation. We will use RIAs and HPLC for biochemical analysis of PGs and LTs.